In the case of something like methicillin resistant staphylococcus aureus - the MRSA you've been hearing so much about lately - the media is like a big echo chamber, magnifying what you hear and distorting it. Reality is different.

Yes, there is a problem. Despite recent news reports of MRSA deaths, this is not a new problem. A medical journal article in 1999 mentioned four fatal cases of MRSA among children in North Dakota and Minnesota during the preceding two years. There is a risk from MRSA and other antibiotic-resistant microorganisms, and it bears talking about because the problem hasn't gone away and won't, and in the meantime there are steps which you should take to protect yourself and the people around you.

Darwin rules

When doctors or scientists talk about resistant organisms, they mean bacteria which aren't affected by most common antibiotics. And the reason why antibiotics are losing effectiveness is because of natural selection and evolution, principles outlined by Charles Darwin 150 years ago.

Expose a population of bacteria to an antibiotic, and some or many or almost all will die. But a few will have a mutated gene which makes the antibiotic ineffective. These bacteria survive and multiply, and soon you have a whole new population of bacteria which your antibiotic won't touch.

Penicillin, the first of the antibiotics, was isolated by the end of World War II, said Carmel Ruffolo, an assistant professor at the University of Wisconsin-Parkside and director of the university's new Center of Health Science. And then it was developed for clinical use over a few subsequent years.

"By about '52, '53, you had microbiologists saying these organisms can become resistant. So the microbiologists knew a long time ago that this was happening. It took the rest of the world another 50 years to catch up, quite literally."

"You know, we stared seeing MRSA back in the 60s," said Dr. Robert Gullberg, an infectious disease specialist with Wheaton Franciscan Healthcare-All Saints. It appeared first in Southeast Asia and spread from there. "When I came to Racine in 1986 we rarely saw a MRSA infection." About 10 years ago, about 5 percent of the staph organisms isolated at St. Mary's hospital were resistant, he said. The fraction was 10 to 12 percent five years ago. "Now we're up to, I believe, approximately 40 percent of our isolates of staph are MRSA." That mirrors what has happened around the country, he said.

And the strains of MRSA found here are the same as those found in other parts of the country, meaning that there is enough movement among people to spread the same strain of bacteria.

"We see women with MRSA infection in their earlobes from pierced ears," Gullberg said "We see high school football players colonized with it, which means the mats are often getting colonized with MRSA."

Most people who have MRSA on their skins don't show any symptoms, Gullberg said. With an estimated 18 to 20 percent of people carrying MRSA, that means up to 38,000 people in the county may carry it, he said, yet what we don't know is why some people with MRSA have symptoms such as boils, while others don't.

Although MRSA is resistant to methicillin, it is still susceptible to other antibiotics. There are about six which doctors can use, Gullberg said. But the laws which Darwin laid down guarantee that at some point these, too will fail. They will because bacteria are very adaptable.

Trading genes

Take penicillin, the first antibiotic and progenitor of a whole line of derivatives. Penicillin works because it blocks the attachment of structural supports which hold a bacteria's cell wall together. Penicillin does this by fitting into the space where the support attaches, like puzzle pieces locking into place. But if a mutation very slightly alters the genetic code for that site penicillin can't lock into place, yet the cell wall support can. Voila, you have a resistant bacteria. And so the search for new antibiotics in part means fussing with the structure of an antibiotic so that it can once more fit into that molecular puzzle.

Other bacteria have other mechanisms to avoid antibiotics. Some pump antibiotics out faster than they can act. Other antibiotics inhibit the replication of DNA, but the bacteria can go on if its enzymes change just enough to inhibit the antibiotic but not DNA replication. In all cases it comes down to genetic modifications. While a natural mutation may start it, bacteria have a few tricks which make them very adaptable.

The first is conjugation. Two bacteria meet and form a bridge and then they trade "plasmids." These are bits of DNA floating around inside the cell separate from the bacteria's chromosomes. Bacteria trade plasmids which the other cell doesn't have. If one happens to be resistant to an antibiotic, that characteristic is transferred, too.

The other is natural transformation. Bacteria can pick up DNA from any spot they land on, Ruffolo said. "At a very low frequency some of these DNA pieces have an antibiotic gene, but … all you need is for it to happen once because bacteria have a really good knack of hanging onto things that help them cause infection. So that gene will more than likely be maintained."

Nature's way

Looking for answers to antibiotic resistance involves looking at nature's example. Leaf-cutting ants grow gardens of fungi for food and also use bacteria which produce antibiotics to defend these fungi gardens. What's fascinating about the ant gardens is that the bacteria in them don't develop resistance despite being exposed to a constant barrage of antibiotics produced by the fungi, said Marcin Filutowicz, a professor of bacteriology at the University of Wisconsin-Madison and one of the people involved in Wispar, the Wisconsin Project for Antimicrobial Research.

Understanding why resistance doesn't happen in this case may give us clues about why it does develop in the bacteria we're used to seeing, he said.

Antibiotics were isolated from bacteria, and the first explanation for their existence was that they were developed by bacteria to kill other bacteria. "But this view seems to (be changing)," Filutowicz said, "and we think antibiotics were developed by bacteria to communicate among themselves. We know that antibiotics at very low, nonthreatening levels change expression of genes in bacteria." The emerging thought is that antibiotics finely tune the workings of genes for other bacteria in the same place. "This is their language. They developed chemistry that allowed them to say, 'Hey, I'm here. Who wants to dance with me?'"

Filutowicz and his colleagues in Wispar are looking for new sources of novel antibiotics or solutions to antibiotic resistance. They are, for example, studying bacteria in the soil, many of which produce their own antibiotics. They're looking for small molecules which could be absorbed by bacteria and which would prevent the duplication of those plasmids, meaning resistance genes would not be passed to the next generation. Filutowicz is the founder of a small biotech company, ConjuGon, which is looking for molecules which stop bacteria from joining and exchanging plasmids. And researchers are looking for molecules which will cause cells to expel plasmids.

Imagine how that might work, Filutowicz said, because many of the genes which make bacteria virulent are also on plasmids. Anthrax bacteria, for example, have only two plasmids which cause virulence. If there is a biological attack alert and we had such a molecule, it could be sprayed in the air to neutralize any anthrax bacteria in the vicinity. A more mundane example: Before getting a dose of antibiotic, a patient would first drink a chemical to neutralize any antibiotic-resistant plasmids.

"You can expel the plasmid. What happens if this thing is on the chromosome?" Ruffolo said. There are examples of DNA on plasmids which becomes part of the bacterial genome and is then not easy to get rid of.

Personally, Filutowicz said, he doubts that researchers will ever find a magic bullet to stop bacteria. Ruffolo is firmly convinced of that. Bacteria are too adaptable, she said. They have backup systems for backup systems, making it unlikely that attacking one target will ever neutralize them. She thinks we should hunt for vaccines which have already saved us from the scourges of several diseases.

It comes down to research money, and both Ruffolo and Filutowicz said the federal government is not doing enough. Big pharmaceutical companies are uninterested because their profit demands mean they wouldn't make money on chemicals which are likely to be specific to particular organisms and sold in small amounts, he said. Thus the gap is being filled by venture capitalists and small companies like his own.

"We need more money for antimicrobial research because we are confronting a perfect storm of antibiotic-resistant bacteria. And you know, I don't want to sound alarmist but if we don't do anything, if we continue relying on existing antimicrobial agents, in 20, 50 years we would confront the situation before antibiotics were introduced to medicine. We will be dying like flies."

Four things you can do

• Wash your hands thoroughly and generally practice good hygiene.

• Don't ask for antibiotics if you have a cold or flu. Antibiotics don't work on viruses.

• Don't demand an antibiotic if your health care provider says it's not necessary.

• If you are given an antibiotic, take all of it. Don't stop just because you feel better.